Diabetes mellitus is a chronic multisystem disease in which all types of metabolism are disrupted.It is characterized by impaired secretion or action of insulin, accumulation of glucose in the blood (hyperglycemia), urine (glucosuria) and the development of complications.
The modern clinic employs endocrinologists with many years of experience in the field of endocrinology.Doctors will be able to correctly determine the degree of compensation for diabetes mellitus, identify existing complications and prescribe or adjust a treatment program.
How does glucose metabolism normally occur?
Glucose is the body's main source of energy.It enters the body with food, mainly with carbohydrates, or is synthesized by a series of metabolic reactions from fats and proteins.Excess glucose accumulates in the liver and muscles as glycogen and is used as needed.
All tissues of the human body are divided into insulin-dependent (muscles, adipose tissue, cardiomyocytes) and non-insulin-dependent (brain, red blood cells, cornea, liver, kidneys).In order for glucose to pass into the cell from insulin-dependent tissue and be used in cellular metabolism, insulin is necessary.It is produced in the β cells of the pancreas.Insulin acts like a key that opens the lock allowing glucose to enter the cell.Insulin-independent tissues receive glucose by simple diffusion, passively.
When everything works correctly in the body, the process of glucose penetration into insulin-dependent tissues occurs dynamically and no problems arise.When the production of insulin is disrupted (for example, when the pancreas is damaged) or the mechanism of its action on the cell is disrupted (the cellular "lock" is broken), glucose begins to accumulate in the body and cellular starvation develops in the cells.
Below we'll look at what happens when glucose builds up in the body and the different types of diabetes.
Ranking
Experts distinguish several main types of diabetes.We will focus on the four most common:
- Type I (former name: insulin dependent);
- Type II (former name: insulin-independent);
- Gestational;
- Symptomatic.
Let's look at each type in more detail.
Type I diabetes mellitus
This type of diabetes mellitus develops as a result of damage to the β cells of the pancreas, the source of insulin in the body, which leads to a state of absolute insulin deficiency.One of the common causes of cell damage is the development of an autoimmune process, when pancreatic cells begin to be perceived by the body as foreign.Antibodies build up against them, completely destroying the source of insulin.
Other causes of pancreatic beta cell destruction:
- effects of chemicals (nitrosamine, pesticides, certain medications);
- infectious lesion (measles, rubella virus, cytomegalovirus);
The disease develops when more than 80% of cells are destroyed.
Type I diabetes mellitus is typical for young people and often begins at an early age, in an acute form, with a rapid increase in clinical symptoms.
Type II diabetes mellitus
Diabetes mellitus type II (former name: insulin-independent) develops as a result of a violation of the receptor apparatus of cells, due to which insulin resistance is formed in the body.
In this type of diabetes mellitus, insulin is produced in the required volume, but insulin-dependent cells stop responding to it.Relative insulin deficiency leads to decreased glucose utilization by muscles and adipose tissue, which contributes to the development of hyperglycemia.
The causes of type II diabetes are:
- hereditary predisposition;
- overeating, obesity;
- physical inactivity;
- chronic stress state.
Table 1. Comparative characteristics of type I and type II diabetes mellitus.
| Sign |
Type I |
Type II |
| Prevalence |
15% |
85% |
| Onset of illness |
Most often in childhood or adolescence |
Middle age and old age |
| Acute |
Long-term progressive |
|
| Development of symptoms |
Fast |
Slow |
| Phenotype (appearance) |
Skinny |
Obesity |
| Insulin level |
Missing |
Increase |
| Insulin resistance |
- |
+ |
| Insulin deficiency |
Absolute |
Parent |
| Ketoacidosis |
+ |
- |
Gestational (diabetes during pregnancy)
Physiological pregnancy is characterized by two significant changes in glucose metabolism:
- Constant supply of glucose to the placenta and fetus.During pregnancy, due to increased consumption of glucose, its level in the body decreases faster than in a non-pregnant woman.
- A decrease in tissue sensitivity to insulin during the second trimester of pregnancy, leading to the formation of insulin resistance.
This condition is caused by an excess of hormones: progesterone, cortisol, prolactin, which have a counter-insular effect (block the action of insulin).This reduces the sensitivity of fat and muscle tissues to insulin.
Physiological pregnancy is characterized by both insulin resistance and a compensatory increase in pancreatic β-cell function, which helps maintain optimal glucose metabolism.In women with glucose intolerance, the compensatory capacities of β cells are insufficient, which leads to the formation of hyperglycemia.
Diagnosis of gestational diabetes mellitus
In order to reduce the risk of complications for both the mother and the fetus, it is necessary to correctly diagnose and correct gestational diabetes mellitus.
The diagnosis is carried out in 2 phases:
- The first phase is carried out when a pregnant woman first consults a doctor before 24 weeks of pregnancy.A woman undergoes one of the tests: venous blood donation on an empty stomach, glucose tolerance test or determination of glycated hemoglobin HbA1c.
- The second phase is carried out in pregnant women in whom carbohydrate metabolism disorders have not been identified at an early stage.Diabetes mellitus is diagnosed by performing a glucose tolerance test with 75 g of glucose between 24 and 28 weeks of pregnancy.
La norme de glycémie à jeun chez la femme enceinte est inférieure à 5,1 mmol/l. Au bout d'une heure, lors d'un test oral d'hyperglycémie provoquée, les valeurs normatives sont inférieures à <10,0 mmol/L, et au bout de 2 heures supérieures à 7,8 mmol/L et inférieures à 8,5 mmol/L.
Pathological indicators of venous blood glucose are the following values:
- fasting, more than 7.0 mmol/l;
- glycated hemoglobin (HbA1) greater than 6.5%;
- blood sugar is above 11.1 mmol/l (time of day and last meal do not matter).
These cases indicate the manifestation of gestational diabetes mellitus and require immediate insulin therapy.
High fasting values that do not correspond to the parameters of manifest diabetes - above 5.1 mmol / l, but below 7.0 mmol / l, place the pregnant woman in a group at increased risk of diabetes.Such women are advised to undergo rational diet therapy, dynamic control of glycemic levels and the condition of the fetus.
Symptomatic diabetes mellitus
This type is secondary and is caused by impaired glucose metabolism due to various diseases or medications.These conditions include:
- diseases of the exocrine pancreas (pancreatitis, cancer, cystic fibrosis);
- medicated diabetes mellitus - when taking glucocorticosteroids (have a counter-insular effect, reduce the production of insulin in the body), phenytoin, estrogens (oral contraceptives).
Symptomatic diabetes mellitus can usually be treated by addressing the underlying cause of the diabetes (for example, by changing or stopping a medication).
Why is high blood sugar bad?
We have already understood that a lack or dysfunction of insulin leads to a buildup of glucose in the blood.When the renal threshold is reached (>8.8 mmol/l - value at which the kidneys begin to evacuate glucose during blood filtration), glycosuria develops.Glucose is an osmotically active substance, so it binds water and leads to polyuria, loss of large amounts of water from the body and compensatory activation of the thirst center.
Polyuria (excretion of a large volume of urine in large portions) leads to dehydration of the body, a decrease in blood volume in the bloodstream, a decrease in blood pressure and hypoxia of tissues located on the periphery.This carries a risk of thromboembolism and development of disseminated intravascular coagulation syndrome.
In addition, the pressure drop is less than 50 mm.art.Art.leads to a slowdown in renal blood flow, which can lead to anuria (lack of urination) and the development of acute renal failure.
There is a peculiarity in the pathogenesis of type I diabetes mellitus - absolute insulin deficiency leads to the activation of contrainsular hormones (insulin antagonists): T4, adrenaline, cortisol, somatotropic hormone, glucagon.
The following hormones improve all types of metabolism, leading to an even greater increase in glucose:
Lipolysis is the destruction of fats, which leads to the formation of large amounts of free fatty acids (FFA), and from them, glucose.
FFAs are an alternative source of energy in the body, serving as a basis for the formation of ketone bodies (e.g., acetone).An increase in ketones in the blood and urine causes vomiting, metabolic acidosis (decrease in blood pH), and compensatory hyperventilation of the lungs (noisy, deep acidotic Kussmaul breathing occurs).The accumulation of ketones leads to one of the serious complications - ketoacidosis coma.
- Gluconeogenesis is a metabolic pathway by which glucose is synthesized from non-carbohydrate sources (amino acids, fatty acids).
- Glycogenolysis is the process of breakdown of glycogen (glucose storage in the liver).
Symptoms
We have dealt with the main links in the pathogenesis of diabetes mellitus, now we will describe the clinical symptoms by which this disease can be suspected:
- thirst (polydipsia) - associated with dehydration of the body;
- frequent urination (polyuria) - is due to the fact that glucose is osmotically active and binds water;
- increased appetite - is due to the fact that glucose does not enter the cells, a state of energy starvation is formed there;
- dry skin, peeling, itching - these symptoms appear as a result of dehydration and dysfunction of the sweat and sebaceous glands;
- pustular skin diseases - result from a decrease in the body's resistance;
- weakness, depressed mood.
Early complications
Early complications are acute conditions characterized by a rapid increase in clinical symptoms and requiring immediate medical intervention by a physician.
Early complications of type I diabetes
- Ketoacidosis coma is observed more often in the first type of diabetes mellitus.It is characterized by a pungent, “fruity” mouth odor, depression of consciousness, weakened reflexes, diarrhea, nausea, and ketoacidotic Kussmaul respiration.
Other complications are also characterized by depression of consciousness, reflexes and a decrease in blood pressure:
- Hyperosmolar coma
- Lactic acidotic coma
- Hypoglycemic coma
Differential diagnosis of the type of coma is carried out using a biochemical analysis of blood, urine and the acid-base state of the blood.
Early complications of type II diabetes
- Hyperosmolar coma - observed more often
- Lactic acidotic coma
- Hypoglycemic coma
Late complications
These include:
- microangiopathies: retinopathy, nephropathy;
- macroangiopathies: coronary heart disease, angina pectoris, atherosclerosis, hypertension, chronic cerebral ischemia, acute stroke;
- neuropathies (polyradiculoneuropathy, radiculopathy, lumbar plexopathy);
- sorbitol deposition in tissues (cataracts);
- immunodeficiencies: pustular diseases, prolonged tissue healing);
- diabetic foot - pathological changes in the peripheral nervous system, arterial and microcirculatory beds, osteoarticular apparatus of the foot with the development of ulcerative-necrotic processes and gangrene.
Mechanisms of late complications
Late complications of diabetes are mainly associated with damage to blood vessels.Their main mechanism is the glycosylation of all protein structures in the body (vascular endothelium, basement membrane, nerve ending vessels).
Glycosylated proteins:
- increase the permeability of the vascular wall and disrupt the rheological properties of blood, which causes the development of thrombosis;
- promote the production of pro-inflammatory factors that damage small capillaries;
- block vasodilation;
- increase lipid peroxidation, which leads to the production of reactive oxygen species that damage tissues;
- contribute to the development of endothelial dysfunction and increase the risk of atherosclerosis.
As a result of these processes, the walls of small vessels become rigid, inelastic and prone to rupture.The speed of blood flow in small vessels slows and the viscosity of the blood increases.
Cataract
Cataract is one of the most common late complications of diabetes mellitus.
It is formed due to the fact that excess glucose enters alternative metabolic pathways.One of these pathways is the polyol oxidation pathway to sorbitol.Sorbitol is a compound that increases osmotic pressure in the eye cavities and causes clouding of the lens.
Diabetic glomerulosclerosis
This nephropathy is accompanied by morphological changes in the capillaries and arterioles of the renal glomeruli, leading to their closure (occlusion), sclerotic changes, a progressive decrease in the filtration function of the kidneys and the development of chronic renal failure.
Diabetic neuropathy and retinopathy
Diabetic neuropathy is characterized by damage to the central and peripheral nervous system, which is clinically manifested by impaired sensitivity.
Diabetic retinopathy is characterized by damage to the capillaries, arterioles and venules of the retina with the development of microaneurysms, hemorrhages, exudative changes and the appearance of newly formed vessels.
Diabetes treatment
Type 1 diabetes mellitus is treated with insulin.Insulin, depending on its duration of action, is divided into:
- ultra-short action - used before each meal.Onset of action 5 to 15 minutes, duration 2 to 5 hours;
- short-acting - used before each meal.Starts working after 30 minutes and lasts 5-8 hours;
- average duration of action - begins to act in 1-2 hours, the duration of action is 18-24 hours.Necessary for the occurrence of basic energy processes;
- prolonged action - begins to act after 1-2 hours, duration 18-36 hours.Necessary for the occurrence of basic energy processes.
Doctors treat type II diabetes mellitus in 3 stages.
1st stage of treatment:
- in people with normal body weight - diet therapy (limiting foods rich in carbohydrates);
- For overweight people, obesity therapy is carried out: more active diet therapy (strict limitation of the total calorie content of food, carbohydrates and animal fats), physical (therapeutic) activity in a regular dose, lifestyle changes, involving an increase in physical activity at home and during leisure time.
2nd stage of treatment:
- the use of drugs that stimulate β cells: sulfonylurea derivatives, biguanides;
- the use of drugs that increase the sensitivity of insulin receptors in muscles and adipose tissue: thiazolidinediones.
Stage 3 of treatment: insulin therapy.
Principles of treatment in an emergency
Ketoacidosis coma:
- insulin and glucose replacement therapy;
- restoration of fluid volume, electrolytes and blood pH.
Hyperosmolar coma:
- restoration of fluid volume and osmotic blood pressure by administering hypotonic (0.45%) sodium chloride solution (2-3 liters);
- administration of electrolytes with short-acting insulin preparations in small doses (5-10 U/hour).
Benefits of in-clinic treatment
- Doctors will conduct a thorough diagnosis of the body to detect the presence of diabetes and its complications for treatment.
- We will select an individual treatment program based on the latest clinical recommendations and the many years of clinical experience of doctors.
- Doctors will provide the patient with detailed advice on the recommendations and rules that people with diabetes should follow.